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J. Biol. Chem., Vol. 281, Issue 8, 4624-4637, February 24, 2006

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The 2',5'-Oligoadenylate Synthetase 1b Is a Potent Inhibitor of West Nile Virus Replication Inside Infected Cells^*

Anna Kajaste-Rudnitski¹², Tomoji Mashimo³, Marie-Pascale Frenkiel, Jean-Louis Guénet, Marianne Lucas¹⁴, and Philippe Desprès⁵

From the Interactions Moléculaires Flavivirus-Hôtes and Génétique des Mammifères, Institut Pasteur, 25 Rue du Dr. Roux, 75724 Paris, Cedex 15, France

The 2',5'-oligoadenylate synthetase (OAS) proteins associated with endoribonuclease RNase L are components of the interferon-regulated OAS/RNase L system, which is an RNA decay pathway known to play an important role in the innate antiviral immunity. A large body of evidence suggests a critical role for the 1b isoform of the mouse Oas gene (Oas1b) in resistance to West Nile virus (WNV) infection in vivo. WNV is a positive, single-stranded RNA virus responsible for severe encephalitis in a large range of animal species and humans. To investigate the molecular basis for the sensitivity of WNV to the Oas1b antiviral pathway, we established a stable mouse fibroblastic cell clone that up-regulates Oas1b protein expression under the control of the Tet-Off expression system. We showed that murine cells respond to Oas1b expression by efficiently inhibiting WNV replication. The antiviral action of Oas1b was essentially restricted to the early stages in virus life cycle. We found that the inability of WNV to productively infect the Oas1b-expressing cells was attributable to a dramatic reduction in positive-stranded viral RNA level. Thus, Oas1b represents an antiviral pathway that exerts its inhibitory effect on WNV replication by preventing viral RNA accumulation inside infected cells.

Received for publication, August 5, 2005 , and in revised form, December 21, 2005.

^* This work was supported in part by grants from the Institut Pasteur's Programme Transversal de Recherche. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. This work is dedicated to J. L. Guénet for his retirement.

¹ Both authors contributed equally to this work.

² Supported by a fellowship from the Ministere de la Recherche et de la Technologie.

³ Present address: Institute of Laboratory Animals, Kyoto University Graduate School of Medicine, Kyoto 606-850, Japan.

⁴ Supported by a fellowship from the Programme Transversal de Recherche.

⁵ To whom correspondence should be addressed. Tel.: 33-(0)140-613-563; Fax: 33-(0)140-613-774; E-mail: pdespres{at}pasteur.fr.

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